THOC1 binds to U2AF2 and regulates ovarian cancer progression through the beta-catenin / c-myc / cyclinD1 signaling pathway.

BACKGROUND: Ovarian cancer (OV) poses a significant challenge in oncology due to its complex molecular mechanisms and poor prognosis. This study aims to identify key genes associated with OV progression and explore their potential as therapeutic targets. METHODS: Using multiple machine learning models to identify a key gene in OV. Pan-cancer analysis was conducted to evaluate the expression, mutation, diagnosis, prognosis and pathway of THOC1 across various tumors. Cell proliferation, migration, and invasion experiments were performed to assess the role of THOC1 in OV. Immunoprecipitation (IP), GST pull-down, immunofluorescence, and reverse transcription polymerase chain reaction (RT-qPCR) were employed to identify THOC1-interacting proteins. Finally, RNA sequencing and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were utilized to investigate the molecular pathways involving THOC1 and its interaction with U2 Small Nuclear RNA Auxiliary Factor 2 (U2AF2). RESULTS: THOC1 plays an important diagnostic and prognostic role in a variety of tumors and is involved in multiple cancer pathways. Functional assays demonstrated that THOC1 suppresses OV cell proliferation, migration, and invasion. Mechanistically, THOC1 directly binds to U2AF2, with THOC1-340S being a critical interaction site. THOC1 regulates U2AF2 expression, which mediates the suppression of OV progression. RNA-seq and KEGG pathway analysis revealed that THOC1 inhibits the Wnt signaling pathway through its interaction with U2AF2, as evidenced by changes in the protein levels of cyclinD1, c-myc, and beta-catenin. CONCLUSIONS: This study highlights the pivotal role of THOC1 in OV progression and identifies the THOC1-U2AF2 axis as a potential therapeutic target. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12935-025-04034-z.